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Abstract
Clioquinol, one of the first mass-produced drugs, was considered safe and efficacious
for many years. It was used as an antifungal and an antiprotozoal drug until it was
linked to an outbreak of subacute myelo-optic neuropathy (SMON), a debilitating disease
almost exclusively confined to Japan. Today, new information regarding clioquinol
targets and its mechanism of action, as well as genetic variation (SNPs) in efflux
transporters in the Japanese population, provide a unique interpretation of the existing
phenomena. Further understanding of clioquinol’s role in the inhibition of cAMP efflux
and promoting apoptosis might offer promise for the treatment of cancer and/or neurodegenerative
diseases. Here, we highlight recent developments in the field and discuss possible
connections, hypotheses and perspectives in clioquinol-related research.